The Cytoprotective Effects of Baicalein on H2O2-Induced ROS by Maintaining Mitochondrial Homeostasis and Cellular Tight Junction in HaCaT Keratinocytesopen access
- Authors
- Kim, Gyeonghyeon; Han, Dong-Wook; Lee, Jong Hun
- Issue Date
- Apr-2023
- Publisher
- MDPI
- Keywords
- baicalein; antioxidants; tight junction; mitochondrial homeostasis; Nrf2/NQO-1/HO-1 pathway; HaCaT keratinocytes
- Citation
- ANTIOXIDANTS, v.12, no.4
- Journal Title
- ANTIOXIDANTS
- Volume
- 12
- Number
- 4
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/88237
- DOI
- 10.3390/antiox12040902
- ISSN
- 2076-3921
- Abstract
- Reactive oxygen species (ROS) promote oxidative stress, which directly causes molecular damage and disrupts cellular homeostasis, leading to skin aging. Baicalein, a flavonoid compound isolated from the root of Scutellaria baicalensis Georgi has antioxidant, anticancer, anti-inflammatory, and other medicinal properties. We aimed to investigate the protective effect of baicalein on the disruption of tight junctions and mitochondrial dysfunction caused by H2O2-induced oxidative stress in HaCaT keratinocytes. The cells were pretreated with 20 and 40 mu M baicalein followed by treatment with 500 mu M H2O2. The results revealed that baicalein exerted antioxidant effects by reducing intracellular ROS production. Baicalein attenuated the degradation of the ECM (MMP-1 and Col1A1) and the disruption of tight junctions (ZO-1, occludin, and claudin-4). In addition, baicalein prevented mitochondrial dysfunction (PGC-1 alpha, PINK1, and Parkin) and restored mitochondrial respiration. Furthermore, baicalein regulated the expression of antioxidant enzymes, including NQO-1 and HO-1, via the Nrf2 signaling pathway. Our data suggest that the cytoprotective effects of baicalein against H2O2-induced oxidative stress may be mediated through the Nrf2/NQO-1/HO-1 signaling pathway. In conclusion, baicalein exerts potent antioxidant effects against H2O2-induced oxidative stress in HaCaT keratinocytes by maintaining mitochondrial homeostasis and cellular tight junctions.
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